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Figures

In vitro intrinsic membrane properties of striatal neurons and pharmacological characteristics of corticostriatal synaptic potentials are similar for both WT (D2+/+) and D2R-null mice (D2−/−). A, The graph shows the current–voltage relationship obtained from two striatal neurons recorded from a WT (filled circles) or a D2R-null mouse (open circles). Plots were obtained from voltage-clamp experiments, holding the cells at −85 mV and applying positive and negative steps (0.5–3.0 sec duration).Right, Injection of a positive current pulse (0.9 nA) evoked a tonic firing discharge in neurons recorded from either a WT (a) or a D2R-null animal (b). In both experiments the resting membrane potential (RMP; dotted line) was −85 mV. B, The graph shows the pharmacology of the cortically evoked EPSPs recorded in WT (filled circles; n = 6) or in D2R-null mice (open circles; n = 6), either in control medium or in the absence of external magnesium.Bars indicate the time of application of APV (50 μm), CNQX (10 μm), and magnesium-free medium. Right, EPSPs recorded from single experiments in WT (a, c) or in D2R-deficient (b, d) slices, in the presence (a, b) or absence (c, d) of external magnesium. Note that APV (50 μm) reduced the EPSPs only in magnesium-free medium. RMPs were −85 mV (a) and −85 mV (b). In this figure and in the following ones arrows indicate the artifact of the single synaptic stimulation.

Tetanic stimulation of corticostriatal fibers induces LTD in slices obtained from WT mice but LTP in slices prepared from D2R-null mice. A, The graph summarizes the results from extracellular experiments, measuring the field potential amplitude, performed by using either WT (filled circles; n = 11) or D2R-null brain sections (open circles; n = 12). In this figure and in the following ones the tetanus was delivered at time 0. The bottom part of the figure shows traces from two single extracellular experiments performed with WT (a, b) or D2R-null (c, d) brain slices.B, The graph represents the results on the EPSP amplitude obtained from intracellular experiments (WT,n = 11; D2R-null, n = 9). Traces of EPSPs recorded before and after the tetanus from WT (a, b) or D2R-null (c, d) brain sections are represented in the bottom part of the figure. RMPs were −84 mV (a, b) and −85 mV (2c, d).

Effects of APV on synaptic plasticity and postsynaptic action of NMDA in neurons recorded from WT and D2R-null slices. A, APV (50 μm) reversibly prevented the induction of LTP in D2R-null mice (open circles; n = 13) but not the formation of LTD in WT animals (filled circles;n = 9). The bar shows the period of application of APV. Arrows indicate when the tetanic stimulation was delivered. B, The graph shows the dose–response curve for NMDA-induced membrane depolarization obtained from WT (filled circles; n = 5) and D2R-null (open circles; n = 6) slices. NMDA was bath-applied (20–30 sec) in the presence of 1 μm tetrodotoxin. The bottom part of the figure shows membrane depolarizations obtained from a WT slice (left) and from a D2R-null slice (right) after bath application of NMDA. In both cases the RMP was −85 mV.

Effects of SCH 23390 and l-sulpiride on synaptic plasticity recorded in normal medium. A, Intracellular experiments show that the pretreatment of the slices with 3 μm SCH 23390 prevented the formation of LTD in WT slices (filled circles; n = 4), but it did not affect LTP in D2R-null slices (open circles; n = 5). B, Extracellular experiments from WT slices (filled circles; n = 8) show that acute blockade of D2Rs by 1 μml-sulpiride reversibly prevented the induction of LTD but failed to cause LTP. Arrowsindicate when the tetanic stimulation was delivered. C, The traces represent field potentials recorded from WT slices before (a) and 20 min after (b) the tetanus in the presence of l-sulpiride. Traces inc and d show field potentials recorded after the washout of l-sulpiride, respectively, before and 20 min after the second tetanic stimulation.

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